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与纤连蛋白的黏附调节嗜酸性粒细胞上细胞间黏附分子-1的表达。

Adhesion to fibronectin regulates expression of intercellular adhesion molecule-1 on eosinophilic cells.

作者信息

Higashimoto I, Chihara J, Kawabata M, Nakajima S, Osame M

机构信息

Third Department of Internal Medicine, Kagoshima University Faculty of Medicine, Kagoshima, Japan.

出版信息

Int Arch Allergy Immunol. 1999;120 Suppl 1:34-7. doi: 10.1159/000053591.

Abstract

BACKGROUND

Adhesion molecules may play an important role in eosinophilic activation as well as adherence of extracellular matrix (ECM) including fibronectin (FN) in the inflamed focus. Tissue eosinophils expressed inter-cellular adhesion molecule-1 (ICAM-1, CD54), whereas peripheral blood eosinophils did not. The molecular mechanisms of ICAM-1 expression on eosinophils are not clear. We immunologically examined the effect of adherence to FN on the expression of adhesion molecules in an eosinophilic cell line (EoL-1).

METHODS

EoL-1 cells, suspended at a concentration of 2 x 10(6) cells/ml, were cultured at 37 degrees C in BSA or FN-coated 24-well plates. After 4 h, the cells were removed by pipetting, and the expression of adhesion molecules was evaluated by immunofluorescence.

RESULTS

Adherence of EoL-1 to FN enhanced ICAM-1 (CD54) expression on EoL-1 (FN vs. BSA: 84.76 +/- 17.90 vs. 43.73 +/- 7.60, mean fluorescent intensity). Regarding other adhesion molecules on EoL-1 (CD11a, CD18, CD49d), the expression was not significantly augmented by adherence to FN.

CONCLUSIONS

We concluded that the signal via adhesion of FN regulates the expression of ICAM-1 on eosinophilic cells. This study suggests that eosinophilic adhesion to ECM via adhesion molecules plays an important role in the pathogenesis of allergic inflammation through eosinophilic functional changes, including regulation of expressive adhesion molecules such as ICAM-1.

摘要

背景

黏附分子可能在嗜酸性粒细胞活化以及炎症病灶中包括纤连蛋白(FN)在内的细胞外基质(ECM)黏附中发挥重要作用。组织嗜酸性粒细胞表达细胞间黏附分子-1(ICAM-1,CD54),而外周血嗜酸性粒细胞不表达。嗜酸性粒细胞上ICAM-1表达的分子机制尚不清楚。我们通过免疫学方法检测了在嗜酸性细胞系(EoL-1)中,黏附于FN对黏附分子表达的影响。

方法

将EoL-1细胞以2×10⁶个细胞/ml的浓度悬浮,在37℃下于包被有牛血清白蛋白(BSA)或FN的24孔板中培养。4小时后,通过移液器吸出细胞,并用免疫荧光法评估黏附分子的表达。

结果

EoL-1黏附于FN增强了EoL-1上ICAM-1(CD54)的表达(FN组与BSA组:平均荧光强度分别为84.76±17.90和43.73±7.60)。关于EoL-1上的其他黏附分子(CD11a、CD18、CD49d),黏附于FN后其表达未显著增加。

结论

我们得出结论,通过FN黏附产生的信号调节嗜酸性细胞上ICAM-1的表达。本研究表明,嗜酸性粒细胞通过黏附分子与ECM的黏附在变应性炎症的发病机制中起重要作用,这一过程通过嗜酸性粒细胞功能变化实现,包括调节ICAM-1等表达性黏附分子。

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